• Role of cytokines in the myocardial response to injury
• Transcriptional control of cardiac gene expression

• Analysis of gene expression through multiplex RNAse Protection strategies
• Transcriptional analysis via transient transfection
• Adenoviral over-expression of pertinent signaling molecules and transcription factors
• Variety of transgenic animals lacking or over-expressing cytokine receptors and signaling molecules

• Yue P, Massie BM, Simpson PC, Long CS. 1998. Cytokine gene expression increases in non-myocytes from rats with post-infarction heart failure. Am J. Physiol. 275: H250-258.

• Koudssi F, Lopez JE, Villegas S, Long CS. 1998. Cardiac fibroblasts arrest at the G1/S restriction point in response to interleukin-1ß: evidence for IL-1ß induced hypophosphorylation of Rb. J. Biol. Chem. 273:25796-25803.

• Clerk A, Harrison JG, Long CS, Sugden PH. 1999. Pro-inflammatory cytokines stimulate mitogen-activated protein kinases, increase phosphorylation of c-jun and ATF2 and upregulate c-jun protein in neonatal rat ventricular myocytes. J. Mol. Cell. Cardiol. 31:2087-2099.

• Patten M., Wang W, Shakeri S, Burson M, and Long CS. 2000. IL-1ß increases YY1 abundance and DNA-binding activity in cultured cardiac myocytes. J. Mol. Cell. Cardiol (7):1341-1352.

• Kinugawa K, Minobe WA, Wood WM, Ridgway EC, Baxter JD, Ribeiro RCJ, Tawadrous MF, Lowes BA, Long CS, and M.R. Bristow MR. 2001. Signaling Pathways Responsible for Fetal Gene Expression in the Failing Human Heart – Evidence for Altered Thyroid Hormone Receptor Gene Expression in the Failing Human Heart. Circulation 103:1089-94.

• Ng DCH, Long CS, and Bogoyevitch MA. 2001. A role for the ERK and p38 MAP Kinases in Interleukin 1-stimulated delayed STAT3 activation, ANF expression and hypertrophic morphology of cardiac myocytes. J. Biol. Chem. (in press).

• Editorial Board: J. American College of Cardiology
• American Heart Association, Molecular Signaling study section

The overall focus of my research group is on the effects of pro-inflammatory molecules on myocardial growth and gene expression. Several pieces of background information that suggest that these factors may play a significant role in the pathogenesis of several forms of myocardial dysfunction including: (1) cytokines are elevated in several cardiac disease states, (2) cytokines are produced by myocardial cells themselves in response to injury, and (3) the alterations in gene expression seen in response to cytokines resembles the phenotype of the failing heart.

My laboratory is specifically interested in the role played by IL-1 on the remodeling process following myocardial injury. The overall hypothesis of our work is that the intra-cardiac expression of IL-1 is both a marker of, and progression factor for, the transition to decompensated congestive heart failure. Ongoing projects in the laboratory include:

• Evaluation of the targeted disruption of the IL-1 receptor on the response to myocardial injury in vivo
• Effects of the over-expression of a transcriptional target of IL-1 action on the heart in vivo
• Defining the transcriptional mechanisms of IL-1 effects on cultured cardiac myocytes
• Investigation of the effects of cytokines on the phenotype of the cardiac fibroblast in vitro

  To top of page